cardosopedro

Hello.

I'm analyzing the expression of one gene after induction of cell death with a drug. I am using a wild type strain as well as a knockout mutant strain (for a cell signaling protein, in order to check if the activation of the gene was dependent on this signaling pathway). For the analysis I use the wild type control-treated sample as a calibrator, meaning the expression is 1 in this sample. I have these levels of expression:

wild type control: 1
wild type drug: 50
mutant control: 10
mutant drug: 50

In the mutant I also have induction of the gene to the same levels as in the wild type. But if I consider that in the mutant control sample I already have 10 times more expression of the gene than in the wild type, the induction caused by the drug is only 5 (50/10 = 5) whereas in the wild type this is 50 (50/1 = 50).

Should I consider that the mutant has a decreased capacity to induce the gene or not?


Please leave your comments.
Thanks.

Hello.

I started a thread about this subject about one year ago but I can't find it.

I am studying a gene whose function is not described (let's call it gene "Y"). The protein possesses a domain that is found in some transcription factors of the zinc cluster family although no DNA binding domain is found by bioinformatics. In oppostion to the wild type, the knockout mutant for this protein is unable to induce some genes (when cells are treated with a stress) confirming that it is a transcriptional regulator. Interestingly, one of these genes that the mutant is unable to induce (gene "Z") is adjacent to "Y" in the genome (downstream), suggesting some sort of relationship between two genes that are contiguous in the genome. Another coincidence (or maybe not...) is that the gene immediately before in the genome ("X") contains a zinc finger domain known as a binding region for DNA and RNA. However, I could not find so far any functional relationship between X and Y.

I believe that some sort of interesting mechanism of regulation is occurring but since this is not a subject that I am very familiar with, I don't know very well how to approach the problem.

Is anyone aware of such gene relationships?

Help please!!


Thanks.

Hey.

I was going to buy the Ca2+ chelator BAPTA in the tetrapotassium salt form. Then I found BAPTA tetrasodium salt, which is cheaper in a different seller. Is there any difference/advantage between these reagents?


Thanks.

Hey!

Anyone in the forum with experience with lipid peroxidation? Would you say that lipid peroxidation occurs as an early or as a late event following ROS production?


Thank you.